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EN
Recent data indicate that human T lymphocytes can adhere to elastin and respond to co-stimulatory signals of that protein. This reactivity is mediated by non-integrin receptor, elastin binding protein. In addition, another receptor belonging to integrin family may be also involved. T cell interactions with elastin (but not other extracellular matrix proteins) appear to be upregulated in healthy males and at least patients with vasculitis. Interestingly, statins in pharmacological concentrations strongly and selectively block those interactions. Our data point to the potential role of T cell interactions with elastin in immunopathology of vasculitis and atherosclerosis.
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vol. 48
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issue 5
547-555
EN
1307 patients with suppurative bacterial infections caused by multidrug resistant bacteria of different species were treated with specific bacteriophages (BP). BP therapy was highly effective; full recovery was noted in 1123 cases (85.9%). In 134 cases (10.9%) transient improvement was observed and only in 50 cases (3.8%) BP treatment was found to be ineffective. The results confirm the high effectiveness of BP therapy in combating bacterial infections which do not respond to treatment with all available antibiotics.
EN
Beta2-Microglobulin (beta2M) is the light chain of the class I HLA molecule. The serum level of beta2M is elevated in various diseases including lymphoma, inflammation, viral infections and chronic renal dysfunction. The present study addressed the possible influence of beta2M on T lymphocyte activation in vitro. Peripheral blood mononuclear cells from a group of 17 healthy subjects were examined. Stimulation with OKT3 and fibronectin in combination with 30 mg beta2M/dl resulted in a two-fold increase of cell proliferation. A similar effect was observed when OKT3 and collagen I were applied as well as when OKT3 and collagen IV were used as costimulation to T cells. The CD69 expression, measured by flow cytometry was significantly enhanced above the control level (1.52 ? 1.03% vs 33.21 ? 20.26%, p<<0.01, control group and 30 mg beta2M/dl, respectively). Together, these observations suggest that beta2M may play a role in modulating lymphocyte proliferation, possibly through modification of the CD69 molecule.
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